Alzheimer’s disease is the most common form of dementia but remains poorly understood. Accordingly, there has been little success in developing effecting prevention methods and treatments for the condition. Despite these shortcomings, researchers have consistently found significant associations between Alzheimer’s disease and other afflictions, one (or more) of which may eventually prove to be a crucial ingredient in the development of dementia.
A recent study outlines the role that the herpes virus, specifically herpes simplex virus 1 (HSV-1), may play in the causation and progression of Alzheimer’s disease. The author cites over 150 existing pieces of research that support the association, dating back to a 1991 investigation that found HSV-1 was common among elderly patients with Alzheimer’s. Furthermore, they review evidence that treating HSV-1 can significantly reduce the risk of developing the disease.
What is HSV?
The herpes simplex virus is a microorganism that is a cause of viral infections in humans. There are several types of the virus, the most common of which are version 1 (HSV-1) and version 2 (HSV-2). HSV-1 is known for producing oral cold sores, while HSV-2 is usually responsible for genital outbreaks. Both forms of the disease are highly contagious due to the shedding of viral material from the sores. About two-thirds of the global population under 50 years old is estimated to carry HSV-1.
Both HSV-1 and HSV-2 are difficult to treat due to their ability to evade the immune system. Outbreaks of sores occur sporadically, typically lasting for a few weeks and sometimes disappearing for months or even years. The viral infection can be suppressed using medication, but it will remain dormant within the body until reactivation occurs. There is no known cure for either form of the virus.
The Alzheimer’s Connection
Evidence suggests that HSV-1, but not HSV-2, is closely associated with Alzheimer’s disease in people who are genetically predisposed to this form of dementia. The relationship appears to be dependent on the presence of a specific gene, known as the APOE4 allele. This gene variation alone is known to be associated with a significantly higher risk of developing Alzheimer’s disease (up to 30 times greater than without the gene). When both the HSV-1 virus and APOE4 allele are found, the risk factor is multiplied by 12.
Additional research has shed some light on the ways in which HSV-1 may contribute to the formation and progression of Alzheimer’s disease. A popular theory is that the virus may cause damage within the brain as the immune system weakens with old age. Further investigations demonstrated that HSV-1 can actually cause amyloid and tau proteins to abnormally clump and tangle, which is a primary sign of Alzheimer’s disease.
While the existing evidence is not sufficient to claim that HSV-1 causes Alzheimer’s disease, it does appear that the two conditions interact when the APOE4 gene is present. Accordingly, it may be possible to reduce the risk of developing Alzheimer’s disease by treating HSV-1 in people with a genetic predisposition. Early studies suggest that this approach could be effective, as the risk of dementia was significantly reduced in some patients with both HSV-1 and APOE4 by using antiviral medications to suppress HSV activity. While these results are promising, the author cautions that these results were only seen in patients with severe infections, and more research will be needed to verify the usefulness of the approach for all patients.